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Donations to ‘genetic bank’ aid diabetes research

By PHYLLIDA BROWN

A first ‘genetic bank’ for the study of a common disease was launched
in Britain this week. Its purpose is to help scientists to search through
the 23 pairs of human chromosomes to find genes that predispose to the severest
form of diabetes.

Scientists in Oxford and Birmingham, led by John Todd at the John Radcliffe
Hospital, Oxford, have collected blood samples from 100 families around
Britain, all of whom are unusual in having two diabetic children. They have
extracted and purified B cells, a type of white blood cell, from both parents
and the two diabetic children in each family, then treated the cells so
they continue to divide in culture. This provides a permanent record of
each individual’s genetic fingerprint.

Now researchers will be able to study those fingerprints, using gene
markers, to hunt for genes linked with the disease. Once the approximate
location of a gene on a chromosome has been found, scientists can narrow
down the hunt with specific probes.

Diabetes mellitus takes two forms: ins ulin-dependent, or Type I, which
usually begins in childhood, and noninsulin-dependent, or Type II, which
starts in later life, often in overweight people. Type I diabetes is an
autoimmune disease; its incidence in Britain has doubled in the past decade
and now affects 1 in 500 people. Cells of the immune system attack the cells
in the pancreas that produce insulin. Sufferers need regular injections
of insulin.

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There is certainly no single, ‘sledge-hammer’ gene that makes people
diabetic. Rather, says Todd, there are probably several genes that together
increase a person’s risk of developing the disease to as much as 30 per
cent. Even then, diabetes is far from inevitable. If a person also produces
specific autoimmune antibodies, his or her risk increases further, to perhaps
80 or 90 per cent. As yet, no one knows whether such antibodies are also
under genetic control. Other factors in the environment, such as viral infections,
appear to play an important part.

So far, researchers have linked two human genes with Type I diabetes,
but they account for only a small part of the story. One of the genes is
on chromosome II, the other is within the complex family of HLA genes on
chromosome 6. If all the genes responsible could be identified, then people
could be screened and those at greatest risk offered advice, for example
about diet or treatment to reduce the risk. ‘I am optimistic that it should
be relatively feasible to prevent diabetes,’ says Todd.

But hunting down the genes in such a complex disease is a daunting task.
Large numbers of families must be analysed. The genetic bank, which has
been financed mainly by the British Diabetic Association, has been accumulating
data slowly since 1989 but has only now reached enough families to be viable.
Called the BDA-Warren Repository, it is based at the European Cell Bank
at Porton in Wiltshire. Scientists will be able to buy a ‘copy’ of the whole
set of genetic fingerprints for £25 000. The profits will be channelled
into further research. Eventually, the researchers hope to obtain samples
from 200 families. In the US, a smaller ‘bank’ of 30 families’ genes is
being set up by researchers in Chicago. The British researchers are also
sending some of their data there.